Several observations support the hypothesis that increased levels of endogenously released adenosine might have beneficial effects in thrombo-embolic disease of the cerebral vasculature and on the maintenance of the cerebral circulation and thus recovery after cardiac arrest. Adenosine is released by the hypoxic brain; it increases cerebral blood flow by decreasing vascular resistance, and it depresses Ca++ entry into nerve cells. In addition, adenosine inhibits platelet aggregation and thus reduces the vessel-occluding effects of vascular accidents. Levels of endogenous adenosine can be increased either by increasing cellular adenosine release or by decreasing cellular adenosine uptake. Our studies on brain tissue have revealed that morphine increases adenosine release and that several groups of compounds (including phenothiazines, benzodiazepines, steroids and non-steroidal anti inflammatory agents) decrease adenosine uptake. The effects of these drugs on cerebral blood flow has not been studied in any detail and this is the objective of this proposal. The studies will be conducted on cerebral blood flow in rats measured by a direct new technique, and in rabbits using an electromagnetic flow probe on the internal carotid artery. The results of the study should have dramatic significance for the prevention of brain damage as a result of stroke or cardiac arrest.